The major goals of this project are to characterize the host's immune response to helminth infections and to relate the findings to the pathogenesis of clinical disease. Chronic filariasis and schistosomiasis are both characterized by cellular immune hyporesponsiveness to parasite antigens which may play a role in the persistence of the parasite within the host. The mechanisms involved in this hyporesponsiveness include both serum inhibitory factors and mononuclear suppressor cell populations. Profound immunologic hyperresponsiveness of the immediate type (IgE) characterizes the asthma-like trophic eosinophilia syndrome of human filariasis. The most important antigens are those derived from microfilariae. By contrast patients with patent mocrofilaremia are hyporesponsive. Clearance of these microfilariae depends on anti-surface antibodies. In acute schistosomiasis not only is there marked cellular and humoral immune activity but also the presence of large numbers of circulating immune complexes which may be important in the syndrome's pathogenesis. Larval schistosomes (schistosomules) contain the biogenic amine, serotonin. Its uptake mechanisms and metabolic precursors have been defined.